Comparative genomics of Enterococcus faecalis from healthy Norwegian infants

Solheim, Margrete; Aakra, Ågot; Snipen, Lars; Brede, Dag Anders; Nes, Ingolf F.

doi:10.1186/1471-2164-10-194

Cited by 69 publications

(68 citation statements)

References 44 publications

(78 reference statements)

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“…We demonstrated that phage03 deletion resulted in a decline of E. faecalis JH2-2 infectivity both in C. elegans and in G. mellonella larvae. In agreement with previous reports that have described the absence of phage03 in the genome of E. faecalis food isolates (45) and its enrichment among clonal lineages associated with nosocomial diseases (17,40), we detected the presence of phage03 in the genome of CC2 strains E. faecalis V583, MMH594, and HH22. BLAST searches against the available E. faecalis genomes showed that this phage03-like element was also found with a higher incidence in nosocomial isolates whereas it is rarely found in other strains of different origins (see Table S8 in the supplemental material).…”

Section: Discussionsupporting

confidence: 80%

“…The availability of large amounts of whole-genome sequencing data has facilitated in silico comparative analyses of the gene content of enterococcal strains representing a wide spectrum of biotypes, clonal lineages, and isolation sources. As result, these investigations have contributed to the determination of the size and composition of the E. faecalis core genome (40,50), the genetic background for antibiotic resistance (51), and the identification of potential virulence factors that can influence the bacterial lifestyle (16). However, there is still a lack of understanding of how the genetic variation between commensal and nosocomial strains could explain the alleged behavior associated with these.…”

Section: Discussionmentioning

confidence: 99%

“…These combined approaches identified 135 genes present in JH2-2 but absent from the apathogenic strains (see Table S6 in the supplemental material). A large fraction of these genes encode MGEs with high sequence homology to that identified in the E. faecalis V583 genome (40).…”

Section: Elegans Infection By E Faecalismentioning

confidence: 99%

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A Genomic Virulence Reference Map of Enterococcus faecalis Reveals an Important Contribution of Phage03-Like Elements in Nosocomial Genetic Lineages to Pathogenicity in a Caenorhabditis elegans Infection Model

et al. 2015

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eIn the present study, the commensal and pathogenic host-microbe interaction of Enterococcus faecalis was explored using a Caenorhabditis elegans model system. The virulence of 28 E. faecalis isolates representing 24 multilocus sequence types (MLSTs), including human commensal and clinical isolates as well as isolates from animals and of insect origin, was investigated using C. elegans strain glp-4 (bn2ts); sek-1 (km4). This revealed that 6 E. faecalis isolates behaved in a commensal manner with no nematocidal effect, while the remaining strains showed a time to 50% lethality ranging from 47 to 120 h. Principal component analysis showed that the difference in nematocidal activity explained 94% of the variance in the data. Assessment of known virulence traits revealed that gelatinase and cytolysin production accounted for 40.8% and 36.5% of the observed pathogenicity, respectively. However, coproduction of gelatinase and cytolysin did not increase virulence additively, accounting for 50.6% of the pathogenicity and therefore indicating a significant (26.7%) saturation effect. We employed a comparative genomic analysis approach using the 28 isolates comprising a collection of 82,356 annotated coding sequences (CDS) to identify 2,325 patterns of presence or absence among the investigated strains. Univariate statistical analysis of variance (ANOVA) established that individual patterns positively correlated (n ‫؍‬ 61) with virulence. The patterns were investigated to identify potential new virulence traits, among which we found five patterns consisting of the phage03-like gene clusters. Strains harboring phage03 showed, on average, 17% higher killing of C. elegans (P ‫؍‬ 4.4e ؊6 ). The phage03 gene cluster was also present in gelatinase-and-cytolysinnegative strain E. faecalis JH2-2. Deletion of this phage element from the JH2-2 clinical strain rendered the mutant apathogenic in C. elegans, and a similar mutant of the nosocomial V583 isolate showed significantly attenuated virulence. Bioinformatics investigation indicated that, unlike other E. faecalis virulence traits, phage03-like elements were found at a higher frequency among nosocomial isolates. In conclusion, our report provides a valuable virulence map that explains enhancement in E. faecalis virulence and contributes to a deeper comprehension of the genetic mechanism leading to the transition from commensalism to a pathogenic lifestyle. Enterococcus faecalis is a Gram-positive commensal bacterium of the mammalian gastrointestinal (GI) tract (1) and a leading cause of nosocomial infections worldwide (2). In humans, the normal abundance of E. faecalis in the intestinal lumen ranges between 10 5 and 10 8 CFU/g of feces without causing any obvious deleterious effects on the host (3, 4). However, if either perturbations of the host/commensal balance that weaken the host immune system or environmental factors such as use of antibiotics that inadvertently facilitate outgrowth of resistant E. faecalis occur, life-threatening infections might arise. Moreover, the intri...

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

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A Genomic Virulence Reference Map of Enterococcus faecalis Reveals an Important Contribution of Phage03-Like Elements in Nosocomial Genetic Lineages to Pathogenicity in a Caenorhabditis elegans Infection Model

et al. 2015

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“…Furthermore, six out of seven loci were identical to sequence type 16 from an isolate found in a Norwegian infant's fecal sample (39). Consistent with physiological characterization of the latter isolate, we found genes linked to antibiotic transport or modification and genes encoding virulence factors including collagen-binding adhesin, aggregation substance, enterococcal surface protein, gelatinase (gelE), and cytolysin (39). Additional predicted virulence factors included an exfoliative toxin A and a serine protease known to be transcribed with gelE (40).…”

Section: Analyses Of Two Ecologically Distinct Citrobacter Subpopulatmentioning

confidence: 86%

Strain-resolved community genomic analysis of gut microbial colonization in a premature infant

Morowitz

Denef

Costello³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

187

169

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The intestinal microbiome is a critical determinant of human health. Alterations in its composition have been correlated with chronic disorders, such as obesity and inflammatory bowel disease in adults, and may be associated with neonatal necrotizing enterocolitis in premature infants. Increasing evidence suggests that strain-level genomic variation may underpin distinct ecological trajectories within mixed populations, yet there have been few strain-resolved analyses of genotype–phenotype connections in the context of the human ecosystem. Here, we document strain-level genomic divergence during the first 3 wk of life within the fecal microbiota of an infant born at 28-wk gestation. We observed three compositional phases during colonization, and reconstructed and intensively curated population genomic datasets from the third phase. The relative abundance of two Citrobacter strains sharing ~99% nucleotide identity changed significantly over time within a community dominated by a nearly clonal Serratia population and harboring a lower abundance Enterococcus population and multiple plasmids and bacteriophage. Modeling of Citrobacter strain abundance suggests differences in growth rates and host colonization patterns. We identified genotypic variation potentially responsible for divergent strain ecologies, including hotspots of sequence variation in regulatory genes and intergenic regions, and in genes involved in transport, flagellar biosynthesis, substrate metabolism, and host colonization, as well as differences in the complements of these genes. Our results demonstrate that a community genomic approach can elucidate gut microbial colonization at the resolution required to discern medically relevant strain and species population dynamics, and hence improve our ability to diagnose and treat microbial community-mediated disorders.

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“…Here we report the complete genome sequence of the commensal E. faecalis 62, which was isolated from a healthy Norwegian infant (20). This isolate has the multilocus sequence type ST66, which is not part of any clonal complex related to nosocomial infections (20).…”

mentioning

confidence: 99%

Complete Genome Sequence of the Commensal Enterococcus faecalis 62, Isolated from a Healthy Norwegian Infant

et al. 2011

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The genome of Enterococcus faecalis 62, a commensal isolate from a healthy Norwegian infant, revealed multiple adaptive traits to the gastrointestinal tract (GIT) environment and the milk-containing diet of breast-fed infants. Adaptation to a commensal existence was emphasized by lactose and other carbohydrate metabolism genes within genomic islands, accompanied by the absence of virulence traits.

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Comparative genomics of Enterococcus faecalis from healthy Norwegian infants

Cited by 69 publications

References 44 publications

A Genomic Virulence Reference Map of Enterococcus faecalis Reveals an Important Contribution of Phage03-Like Elements in Nosocomial Genetic Lineages to Pathogenicity in a Caenorhabditis elegans Infection Model

A Genomic Virulence Reference Map of Enterococcus faecalis Reveals an Important Contribution of Phage03-Like Elements in Nosocomial Genetic Lineages to Pathogenicity in a Caenorhabditis elegans Infection Model

Strain-resolved community genomic analysis of gut microbial colonization in a premature infant

Complete Genome Sequence of the Commensal Enterococcus faecalis 62, Isolated from a Healthy Norwegian Infant

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